Hemodynamic coupling between a primary atherosclerotic plaque and subsequent secondary lesions

Abstract

Atherosclerosis is one of the most common diseases of the arterial tree, especially in the coronary arteries. Stenoses exceeding 50% area reduction are shown to alternate the downstream coronary flow, and hemodynamics will lead to further atherogenesis. Clinical evidence also confirms that vascular stenoses are not stagnant since they are usually associated with downstream lesions. In this study, it is hypothesized that the formation of secondary plaques, or aneurysms downstream of a primary stenosis, compensates for the abnormal ranges of hemodynamic forces caused by the primary stenosis. An experimental setup captured the hemodynamics of non-Newtonian blood flow in three-dimensional (3D) printed phantoms of coronary arteries with various sequences of lesions. Then, based on the collected data, in silico models of these lesions were simulated using computational fluid dynamics. For the proposed cases, time-averaged wall shear stress, velocity profile, oscillatory shear index, and relative residence time were extracted at the plaque side and the plaque front walls and compared to the reference model with only the primary plaque. The secondary plaque postulated the abnormal hemodynamic conditions to its downstream, which implies endothelial activation and onset of further pathologic events. However, the secondary aneurysm restored flow conditions to normal after its distal shoulder, preventing more damage to the endothelium. Examined angiograms of patients with developed atherosclerotic lesions unveiled that a sequence of plaques is formed over time, and most interestingly, the series stopped after the formation of an aneurysm.